Combating the costly issue of chronic mental illness disability

Mixing pharmacology with genomics can lead to better results in the workplace

Combating the costly issue of chronic mental illness disability

HR often faces seemingly insurmountable challenges where chronic mental illness is concerned.

At least 15 per cent of Canadians in the workforce will suffer from mental illness during their lifetimes, according to a 2012 Mental Health Roundtable Report produced by Statistics Canada and the Centre for Addiction and Mental Health (CAMH) in Toronto. 

Normally, this type of illness is treated using mental illness medications (MIMs). But often, these medications don’t work effectively and they have side effects. This means that many working Canadians are likely to experience serious problems with their MIMs. 

These can lead to reduced productivity, increased absenteeism, chronic mental health disabilities and even death.

Combining genomics and pharmacology

Fortunately, there is a solution — pharmacogenomics, the combining of pharmacology with genomics. The pharmacogenomics field studies the role of the genome in drug response. The genome of an organism is the whole of its hereditary information encoded in its DNA. 

More specifically, pharmacogenomics analyzes how the genetic makeup of an individual affects their response to drugs. Its goal is to find the right drug at the right dose for the right patient. 

But why is this goal so difficult to achieve? The answer is simple: Mental illness is a disease of the brain, by far the most complex organ in the human body. The brain regulates our actions, thoughts, memory, emotions and more. It does this through neurotransmitters — chemical substances that transmit nerve impulses across junctions to other nerves. 

Different neurotransmitters have different jobs and they work using “pathways.” The cause of mental illness is the presence of abnormal levels of neurotransmitters in one or more pathways. The treatment is to prescribe mental illness medications that help correct these abnormal neurotransmitter levels. 

Each MIM is designed to “target” genes in a specific brain pathway, referred to as “receptors.” But before arriving at their targets, these drugs must be metabolized correctly by another set of genes. Unfortunately, in an individual suffering from mental illness, these metabolic and receptor genes are abnormal because they have mutated.  

It is these mutations in the metabolic and receptor genes that result in the failure of mental illness medications. Unfortunately, unlike blood sugar or cholesterol, mutations in genes cannot be tested using regular pathological tests. Because of this, physicians must resort to a trial-and-error process when prescribing MIMs. 

When medications fail

Historically, these medications have generally failed between 40 and 50 per cent of the time, according to a 2016 European College of Neuropsychopharmacology study on why antidepressants don’t work in some patients. 

And many people possess MIM genetic mutations that will complicate prescribing MIMs. This explains why so many mental illness medications fail when they are first prescribed.  

Historically, pharmacogenomics owes its existence to an international scientific research undertaking (from 1990 to 2003) by the Human Genome Project (HGP). Its goal was to determine the sequence of base gene pairs that make up human DNA and to identify and map all the genes of the human genome from both a physical and functional standpoint. 

Today, the pharmacogenomics field offers a new perspective on preventing chronic mental illness disability. It has made possible genetically driven drug compatibility tests that can pinpoint mutations (abnormalities) in brain genes. 

This information can be used to identify which medications will work best for a patient, which are likely to be ineffective and which may cause serious side effects such as anxiety, heart palpitations or nausea. 

Pharmacogenomic testing can be integrated into modern mental health practices to help select psychotropic drugs — capable of affecting the mind, emotions and behaviours — for individuals who have failed first-line evidence-based treatments, according to astudy by  published by Cambridge University Press. This can yield better symptomatic outcomes, better dosing and a reduced cost of treatment.

Case study shows results

Closer to home, a leading Canadian firm in the personalized prescription field recently carried out an anecdotal, observational study of 89 employees who took a pharmacogenomics test. All were on short-term disability due to depression, anxiety or other mental illnesses. 

The results included the following:

•  Almost all the employees had a significant number of mutated MIM genes that led to their becoming disabled.

•  Following their pharmacogenomic analysis and subsequent personalized genetically driven drug compatibility report, these employees were prescribed correct medications and dosages. 

•  Most employees reported being very satisfied with the genetic test and confirmed that the change in mental illness medications helped them return to work after a shorter period of time than originally expected. 

How, then, can HR leaders help those workers who will experience serious problems with their mental illness medications? Make pharmacogenomics testing available to these employees after they have experienced MIM drug failures. The test can pinpoint the mutations in an employee or a dependant’s MIM genes. 

As well, a pharmacist’s recommendations accompanying a genetically driven drug compatibility report will assist the patient’s physician in identifying drugs to avoid and the best drugs to prescribe in terms of efficacy and side effects.

As a corollary, HR has a responsibility to investigate integrating coverage for pharmacogenomic testing to help employees with mental illness to improve productivity, reduce absenteeism and avoid chronic mental health disabilities.

Sanjida Ahmed is a geneticist at Personalized Prescribing in Toronto. He can be reached at (647) 943-0210 ext: 263 or [email protected]. For more information, visit

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